Abstract

The CA1 region of the hippocampus is a model system for the study of long-term synaptic plasticity, which is thought to play an important role in learning and memory. Specifically, studies of long-term potentiation (LTP) and long-term depression (LTD) have provided many insights into the molecular processes that govern long-term synaptic modifcations. While many signalling molecules have been implicated in the regulation of synaptic plasticity, the cyclic-adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) has proven to play a vital role (Nguyen & Woo, 2003). In particular, PKA enhances LTP through downstream phosphorylation events and gene regulation (Nguyen & Woo, 2003). Conversely, PKA activation inhibits LTD (Nguyen & Woo, 2003).

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